Johnston W E, Vinten-Johansen J, Klopfenstein H S, Santamore W P, Little W C
Department of Anesthesia, Wake Forest University Medical Center, Winston-Salem, North Carolina 27103.
Cardiovasc Res. 1990 Aug;24(8):633-40. doi: 10.1093/cvr/24.8.633.
The aim was to determine whether depressed myocardial contractility is responsible for the decline in stroke volume that occurs with cardiac tamponade.
Left ventricular contractile performance was assessed before and after beta adrenergic blockade using the end systolic pressure-volume relation, the left ventricular dP/dtmax-end diastolic volume relation, and the left ventricular stroke work-end diastolic volume relation during acute cardiac tamponade in dogs.
In eight pentobarbitone anaesthetised dogs (15.7-24.8 kg), transducer tipped and volume impedance catheters were positioned in the left ventricle. Through a median sternotomy incision, a pericardial catheter was inserted to produce varying stages of cardiac tamponade. By the use of transient bicaval occlusions, variably loaded pressure-volume loops were recorded.
Incremental tamponade reduced mean arterial pressure from 105(SEM 3) to 89(2) mm Hg (mild tamponade), 75(2) mm Hg (moderate tamponade), and 59(10) mm Hg (severe tamponade). The slope of the end systolic pressure-volume relation was 6.3(1.2) mm Hg.ml-1 at baseline and increased slightly to 7.7(1.8), 8.5(1.3), and 9.2(1.5) mm Hg.ml-1 with the progressive levels of tamponade (NS). The role of autonomic reflexes was assessed by repeating the tamponade sequence after beta adrenergic blockade with 10 mg of metoprolol intravenously. The slope of the end systolic pressure-volume relation was reduced by metoprolol, at 4.9(1.0) mm Hg.ml-1 (p less than 0.01), but was not significantly altered by the sequence of tamponade following beta blockade [5.6(0.9), 6.0(1.0), and 5.5(7.0) mm Hg.ml-1, respectively (NS)]. Neither were changes found indicative of depressed contractile function with progressive tamponade in the slopes of the left ventricular dP/dtmax-end diastolic volume and stroke work-end diastolic volume relations.
Left ventricular contractility was not altered during acute cardiac tamponade in an anaesthetised, closed chest canine model. Depressed left ventricular contractile function was not responsible for the observed haemodynamic deterioration.
旨在确定心肌收缩力降低是否是心脏压塞时发生的心输出量下降的原因。
在犬急性心脏压塞期间,使用收缩末期压力-容积关系、左心室dP/dtmax-舒张末期容积关系以及左心室搏功-舒张末期容积关系,在β肾上腺素能阻滞剂给药前后评估左心室收缩性能。
在8只戊巴比妥麻醉的犬(体重15.7 - 24.8千克)中,将带有传感器的导管和容积阻抗导管置于左心室内。通过正中胸骨切开术切口插入心包导管,以产生不同阶段的心脏压塞。通过短暂的双腔静脉闭塞,记录不同负荷下的压力-容积环。
逐渐增加心脏压塞程度使平均动脉压从105(标准误3)毫米汞柱降至89(2)毫米汞柱(轻度压塞)、75(2)毫米汞柱(中度压塞)和59(10)毫米汞柱(重度压塞)。收缩末期压力-容积关系的斜率在基线时为6.3(1.2)毫米汞柱·毫升⁻¹,随着心脏压塞程度的加重,略有增加至7.7(1.8)、8.5(1.3)和9.2(1.5)毫米汞柱·毫升⁻¹(无显著性差异)。通过静脉注射10毫克美托洛尔进行β肾上腺素能阻滞之后,重复心脏压塞过程,以评估自主神经反射的作用。美托洛尔使收缩末期压力-容积关系的斜率降低至4.9(1.0)毫米汞柱·毫升⁻¹(p<0.01),但在β阻滞剂给药后,心脏压塞过程中该斜率无显著变化[分别为5.6(0.9)、6.0(1.0)和5.5(7.0)毫米汞柱·毫升⁻¹(无显著性差异)]。在左心室dP/dtmax-舒张末期容积关系和搏功-舒张末期容积关系的斜率方面,也未发现随着心脏压塞程度加重而出现收缩功能降低的变化。
在麻醉的、开胸犬模型的急性心脏压塞过程中,左心室收缩力未发生改变。左心室收缩功能降低并非所观察到的血流动力学恶化的原因。